Changes in Saccharomyces cerevisiae mRNA abundance following oxidative stress and DNA damage stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe
PROVIDER: GSE12220 | GEO | 2008/10/01
SECONDARY ACCESSION(S): PRJNA113853
REPOSITORIES: GEO
Similar Datasets
Project description:We subjected yeast to two stresses, oxidative stress, which under current settings induces a fast and transient response in mRNA abundance, and DNA damage, which triggers a slow enduring response. Using microarrays we performed a conventional quantification of change in mRNA abundance. Experiment Overall Design: We used Affymetrix microarrays to quantify changes in mRNA abundance following oxidative stress (using hydrogen peroxide) and DNA damage stress (using methyl methanesulfonate) during a three-hour time course (0, 30 min, 60 min, 100 min, 140 min, 180 min).
2008-10-26 | E-GEOD-12220 | biostudies-arrayexpress
Project description:We subjected yeast to two stresses, oxidative stress, which under current settings induces a fast and transient response in mRNA abundance, and DNA damage, which triggers a slow enduring response. Using microarrays, we performed a transcriptional arrest experiment to measure genome-wide mRNA decay profiles under each condition. Genome-wide decay kinetics in each condition were compared to decay experiments that were performed in a reference condition (only transcription inhibition without an additional stress) to quantify changes in mRNA stability in each condition. We found condition-specific changes in mRNA decay rates and coordination between mRNA production and degradation. In the transient response, most induced genes were surprisingly destabilized, while repressed genes were somewhat stabilized, exhibiting counteraction between production and degradation. This strategy can reconcile high steady-state level with short response time among induced genes. In contrast, the stress that induces the slow response displays the more expected behavior, whereby most induced genes are stabilized, and repressed genes destabilized. Our results show genome-wide interplay between mRNA production and degradation, and that alternative modes of such interplay determine the kinetics of the transcriptome in response to stress. Keywords: Four separate time courses
2008-10-01 | GSE12221 | GEO
Project description:For each strain two time courses for mRNA abundance: Oxidative and MMS and two time courses for decay: reference decay and following oxidative stress
2011-07-30 | GSE26829 | GEO
Project description:We subjected yeast to two stresses, oxidative stress, which under current settings induces a fast and transient response in mRNA abundance, and DNA damage, which triggers a slow enduring response. Using microarrays, we performed a transcriptional arrest experiment to measure genome-wide mRNA decay profiles under each condition. Genome-wide decay kinetics in each condition were compared to decay experiments that were performed in a reference condition (only transcription inhibition without an additional stress) to quantify changes in mRNA stability in each condition. We found condition-specific changes in mRNA decay rates and coordination between mRNA production and degradation. In the transient response, most induced genes were surprisingly destabilized, while repressed genes were somewhat stabilized, exhibiting counteraction between production and degradation. This strategy can reconcile high steady-state level with short response time among induced genes. In contrast, the stress that induces the slow response displays the more expected behavior, whereby most induced genes are stabilized, and repressed genes destabilized. Our results show genome-wide interplay between mRNA production and degradation, and that alternative modes of such interplay determine the kinetics of the transcriptome in response to stress. Experiment Overall Design: We used Affymetrix microarrays to measure the decay profiles of all genes following transcription inhibition in four separate experiments. In two reference experiments, only transcription inhibtion was applied. In two other experiments, an additional stress was applied prior to transcription inhibition: oxidative stress (0.3mM hydrogen peroxide) or DNA damage (0.1% methyl methanesulfonate).
2008-10-26 | E-GEOD-12221 | biostudies-arrayexpress
Project description:For each strain two time courses for mRNA abundance: Oxidative and MMS and two time courses for decay: reference decay and following oxidative stress We used Affymetrix microarrays to quantify changes in mRNA abundance following oxidative stress and DNA damage stress and also decay following transcription inhibition with and without oxidative stress. Each of the experiments were done for both strains 211 (wt) and 212 (mutant)
2011-07-29 | E-GEOD-26829 | biostudies-arrayexpress
Project description:- mRNA abundance from wild type grown in LB or M9 (mRNA vs. Genomic DNA) : GSM30231 - GSM30238, GSM30338-GSM30341 - mRNA abundance grown in LB with norfloxacin treatment for 10 min or 30 min (mRNA vs. Genomic DNA): GSM30247-GSM30262 - mRNA abundance from gyrA (D82G) mutant grown in LB (mRNA vs. Genomic DNA):GSM30239-GSM30246 - Transcription profile between wild type and gyrA (D82G) mutant: GSM30330-GSM30337 Keywords: other
2004-09-09 | GSE1730 | GEO
Project description:- mRNA abundance from wild type grown in LB or M9 (mRNA vs. Genomic DNA) : GSM30231 - GSM30238, GSM30338-GSM30341 - mRNA abundance grown in LB with norfloxacin treatment for 10 min or 30 min (mRNA vs. Genomic DNA): GSM30247-GSM30262 - mRNA abundance from gyrA (D82G) mutant grown in LB (mRNA vs. Genomic DNA):GSM30239-GSM30246 - Transcription profile between wild type and gyrA (D82G) mutant: GSM30330-GSM30337
2004-09-09 | E-GEOD-1730 | biostudies-arrayexpress
Project description:There has been increasing interest in the quantification and characterization of messages and proteins at the synapse, due to its importance in neurodegenerative disease, most notably Alzheimer’s disease. Here, we report the transcriptomic and proteomic changes that occur in synaptosomes from frontal cortices of Sod2 null mice. Constitutively null Sod2 mice were differentially dosed with the synthetic catalytic antioxidant EUK-189, which can extend the lifespan of these mice, as well as uncover or prevent neurodegeneration due to endogenous oxidative stress. This approach facilitated insight into quantification of trafficked messages and proteins to the synaptosome. We used two complementary methods to investigate the nature of the synaptosome under oxidative stress; either whole genome gene expression microarrays or mass spectrometry-based proteomics using isobaric tagging for relative and absolute quantitation (iTRAQ) of proteins. We have characterized the relative enrichments of gene ontologies at both gene and protein expression that occur due to mitochondrial oxidative stress in the synaptosome, which may lead to new avenues of investigation in understanding the regulation of the synaptic function in normal and diseased states. As a result of using these approaches, we report for the first time an activation of the mTOR pathway in synaptosomes isolated from Sod2 null mice, confirmed by an upregulation of the phosphorylation of 4E-BP1. mRNA was extracted from synaptosome samples of individual mice from each genotype/treatment group (N=9-11 per group/treatment). 200ng of the purified total RNA was then amplified one round using Ambion’s Illumina RNA Amplification Kit, to prepare cRNA for labeling and hybridization to Illumina’s MouseRef-8 v2.0 expression bead chips as per the manufacturers instructions (Illumina, San Diego, CA, USA).
2012-07-16 | E-GEOD-39372 | biostudies-arrayexpress
Project description:We present InTAC-seq, a method for simultaneous quantification of genome-wide open chromatin and intracellular protein abundance in fixed cells. Using InTAC we directly observe variation in chromatin accessibility and transcription factor motif occupancy driven by differences in transcription factor protein abundance. By purifying bone marrow progenitor cells based on GATA1 protein expression, we establish its role in both functional and epigenetic restriction of erythroid cell identity in human hematopoiesis.
2022-03-10 | GSE167934 | GEO
Project description:The use of genome-wide RNA abundance profiling by microarrays and deep sequencing has spurred a revolution in our understanding of transcriptional control. However, changes in mRNA abundance reflect the combined effect of changes in RNA production, processing, and degradation, and thus, mRNA levels provide an occluded view of transcriptional regulation. To partially disentangle these issues, we carry out genome-wide RNA Polymerase II (“Pol2”) localization profiling in budding yeast in two different stress response time courses. While mRNA changes largely reflect changes in transcription, there remains a great deal of variation in mRNA levels that is not accounted for by changes in Pol2 abundance. We find that genes exhibiting “excess” mRNA produced per Pol2 are enriched for those with overlapping cryptic transcripts, indicating a pervasive role for nonproductive or regulatory transcription in control of gene expression. Finally, we characterize changes in Pol2 localization when Pol2 is genetically inactivated using the rpb1-1 temperature-sensitive mutation. We find that Pol2 is lost from chromatin after roughly an hour at the restrictive temperature, and that there is a great deal of variability in the rate of Pol2 loss at different loci. Together, these results provide a global perspective on the relationship between Pol2 and mRNA production in budding yeast. The array studies consisted of 4 time courses in which the genome-wide location of RNA Polymerase II was mapped via chromatin immunoprecipitation (ChIP) in BY4741 S. cerevisiae cells or in such cells bearing the temperature sensitive mutation rpb1, in response to heat shock at 37 degrees C and/or 1.5 mM diamide. All samples were hybridized as the ChIP sample (Cy3 labeled, channel 1) versus its cognate ChIP input sample (Cy5 labeled, channel 2). The first time course was a heat shock in wild-type BY4741 cells. The second time course was a heat shock in BY4741 rpd1 cells. The third time course was a diamide treatment of BY4741 rpd1 cells. The fourth time course was a 10 minute heat shock in BY4741 rpd1 cells followed by treatment from 15-60 minutes with diamide (3 samples). In the first three time courses the time range is 0-120 minutes (5 samples). A total of 18 arrays were used in this study. No additional replicates or dye-flip experiments were performed.
2010-07-16 | E-GEOD-22675 | biostudies-arrayexpress